Amplification of the chromosome 20q region is associated with expression of HPV-16 E7 in human airway and anogenital epithelial cells
To study the role of human papillomavirus (HPV) infection in the development of genetic instability, we transduced normal human airway and anogenital epithelial cells with various combinations of HPV-16 E6, E7, and the reverse transcriptase component of telomerase (hTERT). Cell lines generated by co...
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| Veröffentlicht in: | Virology (New York, N.Y.) N.Y.), 2005-09, Vol.340 (2), p.237-244 |
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| creator | Klingelhutz, Aloysius J. Qian, Qining Phillips, Stacia L. Gourronc, Francoise A. Darbro, Benjamin W. Patil, Shivanand R. |
| description | To study the role of human papillomavirus (HPV) infection in the development of genetic instability, we transduced normal human airway and anogenital epithelial cells with various combinations of HPV-16 E6, E7, and the reverse transcriptase component of telomerase (hTERT). Cell lines generated by co-expression of E7 with E6 and/or hTERT (i.e., E6/E7, E7/hTERT, and E6/E7/hTERT) exhibited extra copies of chromosome 20 and specific amplification of the 20q12-ter region, whereas those generated without E7 (i.e., hTERT alone or E6/hTERT) did not. Co-expression of hTERT and a dominant-negative version of cdk4 that has been shown to inactivate the retinoblastoma (pRb) pathway also resulted in 20q amplification. Interestingly, extra copies of chromosome 20 were observed in early passage keratinocytes that expressed E7 alone, and microarray expression analysis revealed that genes in the 20q region and on chromosome 5 were specifically upregulated in these cells. Our results indicate that chromosome 20q amplification is an early event that may be specifically caused by expression of E7 through inactivation of the pRb pathway in human epithelial cells. |
| doi_str_mv | 10.1016/j.virol.2005.06.027 |
| format | Article |
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Cell lines generated by co-expression of E7 with E6 and/or hTERT (i.e., E6/E7, E7/hTERT, and E6/E7/hTERT) exhibited extra copies of chromosome 20 and specific amplification of the 20q12-ter region, whereas those generated without E7 (i.e., hTERT alone or E6/hTERT) did not. Co-expression of hTERT and a dominant-negative version of cdk4 that has been shown to inactivate the retinoblastoma (pRb) pathway also resulted in 20q amplification. Interestingly, extra copies of chromosome 20 were observed in early passage keratinocytes that expressed E7 alone, and microarray expression analysis revealed that genes in the 20q region and on chromosome 5 were specifically upregulated in these cells. Our results indicate that chromosome 20q amplification is an early event that may be specifically caused by expression of E7 through inactivation of the pRb pathway in human epithelial cells.</description><identifier>ISSN: 0042-6822</identifier><identifier>EISSN: 1096-0341</identifier><identifier>DOI: 10.1016/j.virol.2005.06.027</identifier><identifier>PMID: 16051300</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adult ; Airway epithelial cells ; Anal Canal ; Cell Line ; Chromosome 20 ; Chromosome Mapping ; Chromosomes, Human, Pair 20 ; DNA-Binding Proteins - genetics ; Epithelial Cells - virology ; Gene Amplification ; HPV ; Human papillomavirus ; Humans ; Immortalization ; In Situ Hybridization, Fluorescence ; Infant, Newborn ; Instability ; Karyotyping ; Keratinocytes ; Keratinocytes - virology ; Male ; Papillomaviridae - genetics ; Papillomavirus ; Respiratory Mucosa - virology ; Telomerase ; Telomerase - genetics</subject><ispartof>Virology (New York, N.Y.), 2005-09, Vol.340 (2), p.237-244</ispartof><rights>2005 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-1d60c672592455b9c47ae1ccb60babd82a5ded5b1214486953f31a1039cb84f93</citedby><cites>FETCH-LOGICAL-c488t-1d60c672592455b9c47ae1ccb60babd82a5ded5b1214486953f31a1039cb84f93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.virol.2005.06.027$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16051300$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Klingelhutz, Aloysius J.</creatorcontrib><creatorcontrib>Qian, Qining</creatorcontrib><creatorcontrib>Phillips, Stacia L.</creatorcontrib><creatorcontrib>Gourronc, Francoise A.</creatorcontrib><creatorcontrib>Darbro, Benjamin W.</creatorcontrib><creatorcontrib>Patil, Shivanand R.</creatorcontrib><title>Amplification of the chromosome 20q region is associated with expression of HPV-16 E7 in human airway and anogenital epithelial cells</title><title>Virology (New York, N.Y.)</title><addtitle>Virology</addtitle><description>To study the role of human papillomavirus (HPV) infection in the development of genetic instability, we transduced normal human airway and anogenital epithelial cells with various combinations of HPV-16 E6, E7, and the reverse transcriptase component of telomerase (hTERT). Cell lines generated by co-expression of E7 with E6 and/or hTERT (i.e., E6/E7, E7/hTERT, and E6/E7/hTERT) exhibited extra copies of chromosome 20 and specific amplification of the 20q12-ter region, whereas those generated without E7 (i.e., hTERT alone or E6/hTERT) did not. Co-expression of hTERT and a dominant-negative version of cdk4 that has been shown to inactivate the retinoblastoma (pRb) pathway also resulted in 20q amplification. Interestingly, extra copies of chromosome 20 were observed in early passage keratinocytes that expressed E7 alone, and microarray expression analysis revealed that genes in the 20q region and on chromosome 5 were specifically upregulated in these cells. Our results indicate that chromosome 20q amplification is an early event that may be specifically caused by expression of E7 through inactivation of the pRb pathway in human epithelial cells.</description><subject>Adult</subject><subject>Airway epithelial cells</subject><subject>Anal Canal</subject><subject>Cell Line</subject><subject>Chromosome 20</subject><subject>Chromosome Mapping</subject><subject>Chromosomes, Human, Pair 20</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Epithelial Cells - virology</subject><subject>Gene Amplification</subject><subject>HPV</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>Immortalization</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Infant, Newborn</subject><subject>Instability</subject><subject>Karyotyping</subject><subject>Keratinocytes</subject><subject>Keratinocytes - virology</subject><subject>Male</subject><subject>Papillomaviridae - genetics</subject><subject>Papillomavirus</subject><subject>Respiratory Mucosa - virology</subject><subject>Telomerase</subject><subject>Telomerase - genetics</subject><issn>0042-6822</issn><issn>1096-0341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcFu1DAQhi0EokvhCZCQT9wSxk7iJAeQqqrQSpXooXC1HGeymVUSp3Z2Sx-g742XXUF74WDZo_n_f2x_jL0XkAoQ6tMm3ZF3QyoBihRUCrJ8wVYCapVAlouXbAWQy0RVUp6wNyFsINZlCa_ZiVBQiAxgxR7PxnmgjqxZyE3cdXzpkdveu9EFNyKXcMc9rvdNCtyE4CyZBVt-T0vP8dfsMYSj9fLmZyIUvyg5Tbzfjmbihvy9eeBmauNya5xoMQPHOZpxoHi0OAzhLXvVmSHgu-N-yn58vbg9v0yuv3-7Oj-7TmxeVUsiWgVWlbKoZV4UTW3z0qCwtlHQmKatpClabItGSJHnlaqLrMuEEZDVtqnyrs5O2ZdD7rxtRmwtTos3g549jcY_aGdIP-9M1Ou122kpZQaqjAEfjwHe3W0xLHqksH-CmdBtgxZlVpW1klGYHYTWuxA8dn-HCNB7fHqj_-DTe3walI74ouvD0_v98xx5RcHngwDjL-0IvQ6WcLLYkke76NbRfwf8BjwTryE</recordid><startdate>20050930</startdate><enddate>20050930</enddate><creator>Klingelhutz, Aloysius J.</creator><creator>Qian, Qining</creator><creator>Phillips, Stacia L.</creator><creator>Gourronc, Francoise A.</creator><creator>Darbro, Benjamin W.</creator><creator>Patil, Shivanand R.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20050930</creationdate><title>Amplification of the chromosome 20q region is associated with expression of HPV-16 E7 in human airway and anogenital epithelial cells</title><author>Klingelhutz, Aloysius J. ; Qian, Qining ; Phillips, Stacia L. ; Gourronc, Francoise A. ; Darbro, Benjamin W. ; Patil, Shivanand R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c488t-1d60c672592455b9c47ae1ccb60babd82a5ded5b1214486953f31a1039cb84f93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adult</topic><topic>Airway epithelial cells</topic><topic>Anal Canal</topic><topic>Cell Line</topic><topic>Chromosome 20</topic><topic>Chromosome Mapping</topic><topic>Chromosomes, Human, Pair 20</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Epithelial Cells - virology</topic><topic>Gene Amplification</topic><topic>HPV</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>Immortalization</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Infant, Newborn</topic><topic>Instability</topic><topic>Karyotyping</topic><topic>Keratinocytes</topic><topic>Keratinocytes - virology</topic><topic>Male</topic><topic>Papillomaviridae - genetics</topic><topic>Papillomavirus</topic><topic>Respiratory Mucosa - virology</topic><topic>Telomerase</topic><topic>Telomerase - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Klingelhutz, Aloysius J.</creatorcontrib><creatorcontrib>Qian, Qining</creatorcontrib><creatorcontrib>Phillips, Stacia L.</creatorcontrib><creatorcontrib>Gourronc, Francoise A.</creatorcontrib><creatorcontrib>Darbro, Benjamin W.</creatorcontrib><creatorcontrib>Patil, Shivanand R.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Virology (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Klingelhutz, Aloysius J.</au><au>Qian, Qining</au><au>Phillips, Stacia L.</au><au>Gourronc, Francoise A.</au><au>Darbro, Benjamin W.</au><au>Patil, Shivanand R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Amplification of the chromosome 20q region is associated with expression of HPV-16 E7 in human airway and anogenital epithelial cells</atitle><jtitle>Virology (New York, N.Y.)</jtitle><addtitle>Virology</addtitle><date>2005-09-30</date><risdate>2005</risdate><volume>340</volume><issue>2</issue><spage>237</spage><epage>244</epage><pages>237-244</pages><issn>0042-6822</issn><eissn>1096-0341</eissn><abstract>To study the role of human papillomavirus (HPV) infection in the development of genetic instability, we transduced normal human airway and anogenital epithelial cells with various combinations of HPV-16 E6, E7, and the reverse transcriptase component of telomerase (hTERT). Cell lines generated by co-expression of E7 with E6 and/or hTERT (i.e., E6/E7, E7/hTERT, and E6/E7/hTERT) exhibited extra copies of chromosome 20 and specific amplification of the 20q12-ter region, whereas those generated without E7 (i.e., hTERT alone or E6/hTERT) did not. Co-expression of hTERT and a dominant-negative version of cdk4 that has been shown to inactivate the retinoblastoma (pRb) pathway also resulted in 20q amplification. Interestingly, extra copies of chromosome 20 were observed in early passage keratinocytes that expressed E7 alone, and microarray expression analysis revealed that genes in the 20q region and on chromosome 5 were specifically upregulated in these cells. 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| ispartof | Virology (New York, N.Y.), 2005-09, Vol.340 (2), p.237-244 |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Adult Airway epithelial cells Anal Canal Cell Line Chromosome 20 Chromosome Mapping Chromosomes, Human, Pair 20 DNA-Binding Proteins - genetics Epithelial Cells - virology Gene Amplification HPV Human papillomavirus Humans Immortalization In Situ Hybridization, Fluorescence Infant, Newborn Instability Karyotyping Keratinocytes Keratinocytes - virology Male Papillomaviridae - genetics Papillomavirus Respiratory Mucosa - virology Telomerase Telomerase - genetics |
| title | Amplification of the chromosome 20q region is associated with expression of HPV-16 E7 in human airway and anogenital epithelial cells |
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